Allergy and Immunology Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Allergy and Immunology Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan; Clinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital, Kanagawa, Japan; Center for Life Science Research, University of Yamanashi, Yamanashi, Japan.
Allergol Int. 2018 Sep;67S:S25-S31. doi: 10.1016/j.alit.2018.05.002. Epub 2018 Jun 15.
We have recently demonstrated that T cell-mediated nasal hyperresponsiveness (NHR) is a representative pathophysiological feature of allergic rhinitis (AR). Although several anti-allergic drugs are used for the treatment of AR, the efficacy of these drugs on T cell-mediated NHR have not been elucidated. In these studies we investigated the effects of dexamethasone (Dex), montelukast (Mk), and chlorpheniramine (Chl) on NHR in antigen-immunized and antigen-specific Th2 cell-transferred mice.
OVA-immunized BALB/c mice were treated with Dex, Mk, or Chl and challenged intranasally with OVA. We then assessed NHR, the number of inflammatory cells in the nasal lavage fluid (NALF), mRNA expression of Th2 cytokines in the nasal tissue, the population of CD3CD4 cells in the nasal lymphoid tissue (NALT), and antigen-specific serum IgE and IgG levels. Antigen-induced NHR and changes in antigen-specific T cells in the NALT were investigated in OVA-specific Th2 cell-transferred mice.
Dex significantly suppressed antigen-induced NHR, inflammatory cell infiltration, and IL-4, IL-5, IL-6, and IL-13 expression in immunized mice. Chl was completely ineffective, and only IL-13 expression was suppressed by Mk. None of these drugs affected IgE and IgG production. Antigen-induced NHR and the increase in antigen-specific T cells in the NALT of Th2 cell-transferred mice were inhibited by Dex, but not by Mk or Chl.
Steroids are effective for the reduction of NHR in AR by suppressing the accumulation of inflammatory cells, especially antigen-specific T cells.
我们最近证明 T 细胞介导的鼻高反应性（NHR）是变应性鼻炎（AR）的代表性病理生理特征。尽管有几种抗过敏药物用于治疗 AR，但这些药物对 T 细胞介导的 NHR 的疗效尚未阐明。在这些研究中，我们研究了地塞米松（Dex）、孟鲁司特（Mk）和氯苯那敏（Chl）对抗原免疫和抗原特异性 Th2 细胞转移小鼠 NHR 的影响。
用 OVA 免疫 BALB/c 小鼠，并用 Dex、Mk 或 Chl 处理，并以 OVA 进行鼻腔内攻击。然后，我们评估了 NHR、鼻灌洗液（NALF）中炎症细胞的数量、鼻组织中 Th2 细胞因子的 mRNA 表达、鼻淋巴组织（NALT）中 CD3CD4 细胞的数量，以及抗原特异性血清 IgE 和 IgG 水平。在 OVA 特异性 Th2 细胞转移小鼠中研究了抗原诱导的 NHR 和 NALT 中抗原特异性 T 细胞的变化。
Dex 显著抑制了免疫小鼠的抗原诱导的 NHR、炎症细胞浸润以及 IL-4、IL-5、IL-6 和 IL-13 的表达。Chl 完全无效，只有 Mk 抑制了 IL-13 的表达。这些药物均未影响 IgE 和 IgG 的产生。抗原诱导的 NHR 和 Th2 细胞转移小鼠 NALT 中抗原特异性 T 细胞的增加被 Dex 抑制，但 Mk 或 Chl 则没有。
类固醇通过抑制炎症细胞，尤其是抗原特异性 T 细胞的积累，有效减少 AR 中的 NHR。
